Disclosures: The two cohort studies included in the analysis were funded by the Japan Heart Foundation, and the Japan Research Promotion Society for Cardiovascular Diseases. No conflicts of interest were declared.

Obesity is associated with an increased risk of sudden cardiac death after myocardial infarction, although the so-called “obesity paradox” is still evident in a lower risk of all-cause mortality, a new analysis suggests.

Researchers reported the results of an observational cohort study using data from two Japanese cohort studies involving a total of 6,216 patients discharged alive after acute myocardial infarction. The study was published in the Journal of the American Heart Association.

They found that obese patients – those with a body mass index of at least 27.5 kg/m2 – had a nearly threefold higher risk of sudden cardiac death within 3 years, compared with patients who had a normal BMI, even after adjustment for age, sex, and risk factors such as multivessel disease, left ventricular ejection fraction, and medications.

However, the obese group also showed lower 3-year all-cause mortality, compared with the reference group, whose BMI was 18.5-22.9 kg/m2, while individuals with a BMI below 18.5 kg/m2 had a 61% higher risk of mortality.

The overall all-cause mortality in the cohort was 10.1%, and the incidence of sudden cardiac death was 1.2%.

“For the primary prevention of [coronary artery disease], obesity is recognized as a potent risk factor and an opportunity for therapeutic intervention to prevent cardiovascular disease,” wrote Tsuyoshi Shiga, MD, of Tokyo Women’s Medical University, and coauthors. “However, recent reports have shown that obesity (high BMI) itself does not present a mortality risk but is associated with a better prognosis (obesity paradox) in CAD patients receiving secondary care; these patients received appropriate therapy, including percutaneous coronary intervention and guideline-based medications such as aspirin, beta-blockers, and statins.”

The increased risk of sudden cardiac death in obese patients after MI was harder to explain.

The authors suggested that obesity itself may increase the risk of ventricular arrhythmias developing, and it is also linked with left ventricular hypertrophy, which can lead to cardiac remodeling. Other reports have found evidence in obese individuals of QT prolongation or an increased late potential, and autonomic disturbances that could trigger arrhythmias.

Although reduced left ventricular ejection fraction is the best available predictor of sudden cardiac death, the authors noted that their study found high BMI to be a risk factor independent of left ventricular ejection fraction.

The authors also raised the question of whether intentional weight loss might be effective in reducing the risk of sudden cardiac death in obese patients after MI, but suggested more research was needed to answer this.

The two cohort studies included in the analysis were funded by the Japan Heart Foundation, and the Japan Research Promotion Society for Cardiovascular Diseases. No conflicts of interest were declared.